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Animal Models of MS Reveal Multiple Roles of Microglia in Disease Pathogenesis
1Program in Neurosciences, Department of Pharmacological Sciences, Stony Brook University, Stony Brook, NY 11794-8651, USA.
Abstract:
Multiple sclerosis (MS) is a progressive inflammatory and demyelinating disease that affects more than 2.5 million people worldwide every year. Current therapies use mostly disease-modifying drugs, focusing on blocking and regulating systemic functions and the central nervous system (CNS) infiltration of immune cells; however, these therapies only attenuate or delay MS symptoms, but are not effective in halting the disease progression. More recent evidence indicated that regulation of inflammation within the CNS might be a better way to approach the treatment of the disease and microglia, the resident immune cells, may be a promising target of therapeutic studies. Microglia activation classically accompanies MS development, and regulation of microglia function changes the outcome of the disease. In this paper, we review the contributions of microglia to MS pathogenesis and discuss microglial functions in antigen presentation, cytokine release, and phagocytosis. We describe data both from animal and human studies. The significant impact of the timing, intensity, and differentiation fate of activated microglia is discussed, as they can modulate MS outcomes and potentially be critically modified for future therapeutic studies.
Insights
Multiple sclerosis (MS) therapies currently delay symptoms but do not halt progression. Targeting microglia, the brain's immune cells, offers a promising new therapeutic strategy for treating MS by regulating central nervous system inflammation.
Area of Science:
- Neuroimmunology
- Inflammatory and Demyelinating Diseases
Background:
- Multiple sclerosis (MS) affects over 2.5 million people globally, characterized by progressive inflammation and demyelination in the central nervous system (CNS).
- Current disease-modifying drugs primarily focus on systemic immune regulation and CNS immune cell infiltration, offering only symptomatic relief and disease delay, not halting progression.
- Emerging evidence suggests that targeting inflammation within the CNS, specifically involving microglia, presents a more effective therapeutic avenue for MS.
Purpose of the Study:
- To review the role of microglia in the pathogenesis of multiple sclerosis.
- To discuss the functions of microglia, including antigen presentation, cytokine release, and phagocytosis, in the context of MS.
- To explore the potential of modulating microglia activation for future therapeutic interventions in MS.
Main Methods:
- Review of existing scientific literature, including data from both animal models and human studies.
- Analysis of microglia's contribution to MS pathogenesis.
- Discussion of factors influencing microglia activation, such as timing, intensity, and differentiation fate.
Main Results:
- Microglia activation is a key feature of MS development, and its regulation can alter disease outcomes.
- Microglia play critical roles in antigen presentation, cytokine release, and phagocytosis, all of which impact MS.
- The characteristics of activated microglia significantly influence the course and severity of MS.
Conclusions:
- Modulating microglia function represents a promising therapeutic strategy for multiple sclerosis.
- Understanding the nuanced roles of microglia in MS pathogenesis is crucial for developing effective treatments.
- Future therapeutic studies should focus on critically modifying microglia behavior to halt MS progression.
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